Case 238: Spontaneous Pneumothorax Secondary to Intrapulmonary Necrobiotic Rheumatoid Nodule

Spontaneous pneumothorax from necrobiotic nodule is rare, with increased morbidity and mortality; familiarity with key imaging findings, including subpleural location, internal cavitation, and presence of bronchial connection, is crucial to making the correct diagnosis.

History

A 54-year-old white woman with a history of rheumatoid arthritis who was taking glucocorticoids and methotrexate presented to the emergency department in December with worsening shortness of breath and chest heaviness for 1 week. She reported additional symptoms of weakness, headache, and arthralgia primarily involving her bilateral hands, wrist, ankles, and feet. She denied experiencing fevers, syncope or presyncope, focal neurologic deficits, chest pain, nausea, vomiting, unintentional weight loss, or recent trauma. Additional medical history included hypertension, asthma, degenerative disk disease, and migraine, all of which were reportedly controlled with medications. This patient had a smoking history of 80 pack-years, but she had quit smoking 2 months prior to presentation. She denied abuse of alcohol or recreational drugs and reported she was up-to-date on her immunizations, including those for pneumonia and flu. Family history was pertinent for breast cancer in her mother, sister, and maternal aunt. The patient reported normal findings at screening mammography and colonoscopy. A physical examination was remarkable for slightly asymmetric breath sounds, which appeared to be diminished on the right side. This patient had multiple joint deformities, most notably in the bilateral metacarpophalangeal joints. Initial electrocardiography findings and cardiac biomarkers were negative. Her complete blood count and basic metabolic profile were unremarkable.

Posteroanterior and lateral chest radiographs were obtained in the emergency department. Subsequently, computed tomography (CT) of the chest was performed.

Imaging Findings

Posteroanterior and lateral radiographs of the chest showed a moderate right pneumothorax without evidence of mediastinal shift or tracheal deviation (Fig 1). Unenhanced CT of the chest in lung window settings showed moderate right-sided pneumothorax with multiple bilateral subcentimeter pulmonary nodules (Fig 2). There was bilateral upper lobe–predominant centrilobular emphysema (Fig 2), which was likely related to the patient’s extensive history of smoking tobacco. Axial evaluation of the thorax with soft-tissue window settings (Fig 3) showed trace right pleural effusion. Right pneumothorax also was seen, with focal mild right lower lobe visceral pleural thickening (Fig 3). Thin-section (0.6-mm) axial reconstructions (Fig 4) of unenhanced CT chest images with lung window settings better show the right lower lobe subpleural cavitary nodule that eroded through the visceral pleura, resulting in the right-sided pneumothorax. CT-guided percutaneous needle biopsy of the cavitary nodule was performed by using an 18-guage core biopsy needle. In addition, pleural fluid was sampled and sent for histopathologic evaluation, including fluid chemistry, cytology, and cell cultures. Pathology specimens (Fig 5) with hematoxylin-eosin staining showed areas of geographic stellate necrobiosis with extensive fibrin deposition surrounded by a palisading histiocytic rim. The nodule also contained a scattered mix infiltrate of lymphocytes, plasma cells, multinucleated giant cells, and occasional eosinophils. Additional specimen studies for fungal and mycobacterial organisms were negative. The pleural fluid chemistry proved to be an exudate, without evidence of malignant cells or infectious organisms. Special stains for rheumatoid factor were positive. These findings enabled us to confirm the suspected diagnosis of intrapulmonary necrobiotic rheumatoid nodule.

Figure 1:

Posteroanterior chest radiograph shows a moderate right pneumothorax (arrow) without evidence of mediastinal shift or tracheal deviation.

Figure 2a:

(a, b) Sequential unenhanced transverse CT images of the chest obtained at different levels with lung window settings show moderate right-sided pneumothorax (arrow) with multiple bilateral subcentimeter pulmonary nodules (arrowhead). There is bilateral upper lobe–predominant centrilobular emphysema.

Figure 3:

Transverse unenhanced CT image of the chest obtained with soft-tissue window settings shows trace right pleural effusion (arrowhead). Moderate right-sided pneumothorax with focal mild right lower lobe visceral pleural thickening (arrow) is noted.

Figure 4:

Thin-section (0.6-mm) axial reconstruction of the unenhanced CT chest image obtained with lung window settings better demonstrates the right lower lobe subpleural cavitary nodule (arrowhead) that eroded through the visceral pleura, resulting in the moderate right-sided pneumothorax (arrow).

Figure 5a:

(a) Pathology specimen shows areas of geographic stellate necrobiosis (*) with extensive fibrin deposition (arrowhead) surrounded by a palisading histiocytic rim (arrow). (Hematoxylin-eosin stain; original magnification, ×40.) (b) High-power magnification of this same specimen more clearly shows a scattered mix infiltrate of lymphocytes (thin black arrow), plasma cells (thin white arrow), multinucleated giant cells (large black arrow), and occasional eosinophils (black arrowhead). These findings are most consistent with a diagnosis of necrobiotic rheumatoid nodules. (Hematoxylin-eosin stain; original magnification, ×100.)

Figure 2b:

(a, b) Sequential unenhanced transverse CT images of the chest obtained at different levels with lung window settings show moderate right-sided pneumothorax (arrow) with multiple bilateral subcentimeter pulmonary nodules (arrowhead). There is bilateral upper lobe–predominant centrilobular emphysema.

Figure 5b:

(a) Pathology specimen shows areas of geographic stellate necrobiosis (*) with extensive fibrin deposition (arrowhead) surrounded by a palisading histiocytic rim (arrow). (Hematoxylin-eosin stain; original magnification, ×40.) (b) High-power magnification of this same specimen more clearly shows a scattered mix infiltrate of lymphocytes (thin black arrow), plasma cells (thin white arrow), multinucleated giant cells (large black arrow), and occasional eosinophils (black arrowhead). These findings are most consistent with a diagnosis of necrobiotic rheumatoid nodules. (Hematoxylin-eosin stain; original magnification, ×100.)

Discussion

Given this patient’s age, clinical history, and immunocompromised state (from methotrexate and glucocorticoid administration), the differential diagnosis for multiple bilateral pulmonary nodules in a middle-aged adult is broad. It includes infectious, inflammatory, and neoplastic conditions. The differential diagnosis is somewhat narrowed by the presence of cavitation in one of the nodules. The initial differential diagnosis of cavitary pulmonary nodule includes, but is not limited to (a) infection by bacteria (Nocardia, Staphylococcus aureus, and Mycobacterium, such as tuberculosis and Mycobacterium avium complex), fungus (such as histoplasmosis and chronic aspergillosis), septic emboli, or virus (such as cytomegalovirus and varicella zoster virus); (b) inflammatory conditions, such as rheumatoid arthritis, sarcoidosis, granulomatosis with polyangiitis, or Langerhan cell histiocytosis; and (c) malignancy, including primary lung cancer (classically, squamous cell lung cancer) and metastatic disease to the lung (classically, breast cancer, colon cancer, and osteosarcoma).

The differential diagnosis can be better sorted on the basis of patient history and radiologic images. Given the subacute onset of symptoms and immunocompromised status, inflammatory and infectious causes lead the differential diagnosis. Rheumatoid arthritis involving the lung parenchyma is well established in the literature, with pleuropulmonary disease reported in up to 50% of patients (1). The presence of pulmonary nodules on chest radiographs is noted in 1%–6% of the patients; however, it is seen in 20% of patients at chest CT (2,3). These nodules can be cavitary in up to 50% of patients (2). Additionally, a clinical history of smoking is another known risk factor that predisposes patients with rheumatoid arthritis to developing necrobiotic pulmonary nodules along with more aggressive arthropathy, which was the case in this patient (3). Although overlap rheumatologic syndromes are known to occur, it is more likely for a patient to have her primary clinical condition progress such that it affects the respiratory system than it is for her to develop a new autoimmune inflammatory condition, such as sarcoidosis or granulomatosis with polyangiitis. Because this patient did not exhibit clinical stigmata of infection (fevers, chills, elevated white blood cell count), this was a less likely diagnosis than was an inflammatory condition. However, infection remained a possibility, as the patient was taking an immunosuppressive agent, which could blunt host immune response to infection. As for the diagnostic possibility of malignancy, the patient did not have a prior known history of malignancy, and there were no clinical signs of malignancy, such as weight loss or cachexia. The patient reported normal findings of recent screening mammography performed at an outside institution; however, given a strong family history of breast cancer and her extensive history of smoking, the possibility of malignancy (breast and lung cancers) was considered.

With the past medical history of rheumatoid arthritis resulting in aggressive arthropathy and negative breast and colon cancer screening history, the differential diagnosis was led by intrapulmonary necrobiotic rheumatoid nodules. Panculture was performed to exclude infection by the aforementioned microorganisms. Additionally, transthoracic echocardiography was performed to exclude endocarditis. Biopsy of the cavitary nodule in the right lower lobe was performed, and pleural fluid was sampled for histopathologic evaluation. The pleural fluid evaluation revealed a pH of 7.16 (range, 7.30–7.40), a glucose level of 56 mg/dL (3.1 μmol/L) (range, 60–139 mg/dL [3.3–7.7 μmol/L]), a fluid protein level of 4.7 g/dL (range, 0.4–2.0 g/dL), and a lactate dehydrogenase level of 826 U/L (13.8 μkat/L) (range, 20–300 U/L [0.33–5.0 μkat/L]); therefore, we confirmed it was an exudate. Fluid cytology demonstrated presence of lymphocytes, without evidence of infectious microorganisms. Histopathologic evaluation of the nodule (Fig 5) with hematoxylin-eosin staining revealed areas of geographic stellate necrobiosis with extensive fibrin deposition surrounded by a palisading histiocytic rim. Also, the presence of a scattered mix infiltrate of lymphocytes, plasma cells, multinucleated giant cells, and occasional eosinophils was noted. Pleural fluid was noted to be positive for rheumatoid factor. These findings are most consistent with necrobiotic rheumatoid nodules (1–6). Additional staining for fungal and mycobacterial organisms was negative. Histopathologic evaluation for primary and metastatic disease was unremarkable.

The patient underwent chest tube decompression for the pneumothorax and received high-dose steroids, leflunomide, and methotrexate. The chest tube placement resulted in no change in the size of the pneumothorax and a persistent air leak; therefore, the tube was removed after 5 days. Follow-up chest radiography performed 1 month later revealed persistent right-sided pneumothorax, despite what was deemed appropriate therapy. Repeat CT after 1 month was performed and showed persistent right-sided pneumothorax, with an interval increase in right pleural effusion and an increase in right pleural thickening (Fig 6). Subsequent CT was performed (images not shown) with the chest tube in place while maintaining negative intrapleural pressure and revealed no change in the size of the pneumothorax. These findings are suggestive of trapped lung, which likely resulted from the persistent inflammation due to rheumatoid pleuritis. The patient underwent decortication of the pleural rind, which led to resolution of the pneumothorax. Subsequently, the patient’s immunomodulating drugs were gradually tapered down to a maintenance dose.

Figure 6:

Axial unenhanced CT image of the chest obtained with lung window settings shows persistent right-sided pneumothorax (*) with interval increase in right pleural effusion (arrow) and increase in right pleural thickening (arrowhead). These findings are suggestive of trapped lung.

Rheumatoid arthritis is the most common systemic autoimmune connective tissue disease, with an estimated prevalence of 1% (3). It most commonly affects adults, it is more common in women than in men (estimated ratio of 3:1), and it is most commonly initially diagnosed in patients aged 20–50 years (3). Extra-articular manifestations of rheumatoid arthritis include splenomegaly, subcutaneous nodules, scleritis, and rheumatoid arthritis–associated vasculitis most frequently affecting the cardiopulmonary systems (3). Extra-articular intrathoracic rheumatoid arthritis effects the pleura, most commonly involving approximately 50% of patients (1), but only 20% of patients have symptomatic pleural disease (3). The most common imaging finding is pleural effusion with or without ipsilateral pleural thickening (3–5). The effusions may persist or recur and may result in trapped lung (3–5). Signs suggestive of trapped lung include visceral pleural thickening, persistent pneumothorax (which may develop after drainage of pleural effusion), presence of loculations, or some combination thereof (3–5). Treatment of trapped lung is conservative, as most patients tend to be asymptomatic; thus, patients are monitored clinically. Decortication is usually reserved for patients with symptomatic trapped lung (3,5).

Pulmonary parenchymal complications of rheumatoid arthritis are seen in approximately 1%–6% of patient on chest radiographs (3,6). The findings generally include presence of a fine reticular pattern mainly in the lower lung zones in early stages of the disease (7). As the disease progresses, these become more coarse and diffuse, and honeycombing may be seen in late stages of the disease process (7.8). On thin-section CT images, 40%–60% of patients may have variable degrees of pulmonary involvement (3,6). These include interstitial pneumonitis and fibrosis, intrapulmonary necrobiotic rheumatoid nodules, bronchiolitis obliterans–organizing pneumonia, obliterative bronchiectasis, and follicular bronchiolitis (3–7). The interstitial pneumonitides are seen in up to 60% of patients with rheumatoid arthritis and can be further subclassified into acute interstitial pneumonia, usual interstitial pneumonia, nonspecific interstitial pneumonia, lymphocytic interstitial pneumonia, and cryptogenic organizing pneumonia on the basis of imaging and histologic findings (3,6,7). Interestingly, only 10% of these patients have any clinical signs or symptoms of interstitial lung disease (3,6–10).

The exact prevalence of rheumatoid lung nodules is not clear, and variable rates of 20%–40% have been reported in various studies (3,6,9,11). The pulmonary nodules are seen more frequently in patients with advanced stages of the disease; however, they do not reflect disease activity (3). Intrapulmonary necrobiotic nodules can be single or multiple and unilateral or bilateral, and they can vary from 0.5 mm to 7.0 cm in size (3,6). These nodules are asymptomatic, they are usually associated with subcutaneous nodules, and they are histopathologically identical to the subcutaneous nodules (3,8). The necrobiotic rheumatoid pulmonary nodules can occur in the lungs before there is clinical evidence of arthropathy, and they can be seen in the absence of rheumatoid factor (6). Histologic evaluation of rheumatoid nodules shows the presence of lymphocytes, macrophages, lymphocytes, and plasma cells around a necrotic core of palisading histiocytes (3,6,9).

On thin-section CT images, the necrobiotic rheumatoid pulmonary nodules are usually peripheral in location, adjacent to interlobular septa, or both. The nodules are mostly well defined and can cavitate in up to 50% of cases (3,6,8,9). Occasionally, a subpleural rheumatoid pulmonary nodule can erode into the pleural space, resulting in pneumothorax, which can be further complicated by bronchopleural fistula (if the airway is involved) and persistent pneumothorax (3,6,8–10), neither of which is present in the current case. Given the patient’s history and clinical findings, identification of several pulmonary nodules, including a larger cavitary pulmonary nodule in direct contiguity with the pleural surface, the most likely diagnosis is a rheumatoid necrobiotic nodule complicated by pneumothorax.

Differentiation of rheumatoid nodules from infectious conditions is important, as undiagnosed infection can prove fatal. Infectious causes can be ruled out by using panculture and serologic markers. Primary or metastatic lung neoplasm is another important differential consideration, especially in patients with a history of smoking tobacco. In patients with lung nodules and a history of rheumatoid arthritis, CT of the chest is the next step to further characterize the nodules and to assess for possible presence of additional nodules (12). Further evaluation is recommended for lung nodules that have increased in size or that are larger than 8 mm, (12). Fluorine 18 fluorodeoxyglucose positron emission tomography imaging is of limited utility, as it may or may not reveal substantial activity in the rheumatoid nodule (12–14).

Patients with rheumatoid arthritis affecting the respiratory system have increased mortality and morbidity, accounting for approximately 20% of all rheumatoid arthritis–related deaths (3). The overall prognosis of necrobiotic rheumatoid intrapulmonary nodules is good, with most nodules resolving spontaneously without complications (12). Glucocorticoids, along with various disease-modifying agents, including methotrexate, cyclophosphamide, and leflunomide, are the initial line of therapy. In resistant or aggressive cases of rheumatoid arthritis, patients receive the biologic agents infliximab (anti-tumor necrosis factor α antibody) and rituximab (anti-CD20 antibody) (12,15–17).

In conclusion, pneumothorax secondary to rheumatoid necrobiotic nodule is an uncommon presentation of a common disease, with increased morbidity and mortality. This complication of rheumatoid arthritis is rare, with fewer than 15 cases having been reported in the literature. Familiarity with the imaging spectrum of necrobiotic nodules, including subpleural location, internal cavitation, and presence or absence of bronchial connection, is critical to making the correct diagnosis.

Congratulations to the 142 individuals and eight resident groups that submitted the most likely diagnosis (spontaneous pneumothorax secondary to intrapulmonary necrobiotic rheumatoid nodule) for Diagnosis Please, Case 238. The names and locations of the individuals and resident groups, as submitted, are as follows:

Individual responses

Nishard Abdeen, MD, Ottawa, Canada

Gholamali Afshang, MD, Tinley Park, IL

Gensuke Akaike, MD, Seattle, WA

Ashwin V. Alexander, MBBS, Thrissur, India

Canan Altay, MD, Izmir, Turkey

Albert J. Alter, MD, PhD, Blanchardville, WI

Ronald S. Arams, MD, Tenafly, NJ

Dean E. Baird, MD, Potomac, MD

Kenneth F. Baliga, MD, Rockford, IL

Patricia Balthazar, MD, Atlanta, GA

Manon N. Braat, MD, Utrecht, the Netherlands

Eric L. Bressler, MD, Minnetonka, MN

Ghislain Brousseau, MD, Charlesbourg, Quebec, Canada

Douglas C. Brown, MD, Virginia Beach, VA

Michael P. Buetow, MD, Okemos, MI

Ian A. Burgess, MD, Manly, Australia

Charles H. Bush, MD, Gainesville, FL

Umit Calkolu, MD, Ankara, Turkey

Phillip M. Cheng, MD, MS, Culver City, CA

Michael H. Childress, MD, Washington, DC

Kira Chow, MD, Los Angeles, CA

Haris Chrysikopoulos, Corfu, Greece

Silvia Cisneros Carpio, MD, Durango, Spain

Martin I. Cohen, MD, Westlake Village, CA

Marco A. Cura, MD, Dallas, TX

Carlos Francisco M. da Silva, MD, Setubal, Portugal

Marc G. De Baets, MD, Collina d'Oro, Switzerland

Peter De Baets, MD, Damme, Belgium

Renata de Oliveira e Silva Brenner, MD, Sao Jose dos Campos, Brazil

Mark C. DeLano, MD, Grand Rapids, MI

Mustafa K. Demir, MD, Istanbul, Turkey

Thaworn Dendumrongsup, MD, Songkhla, Thailand

Mark T. DiMarcangelo, DO, MSc, Cherry Hill, NJ

Robert J. Dym, MD, Teaneck, NJ

Seyed A. Emamian, MD, PhD, Bethesda, MD

Francis T. Flaherty, MD, Ridgefield, CT

Eduardo K. Fonseca, MD, Sao Paulo, Brazil

Akira Fujikawa, MD, Tokyo, Japan

Keita Fujimoto, Gifu City, Japan

Toshihiro Furuta, MD, PhD, Bunkyo-ku, Japan

Parthasarathy Ganesan, New Delhi, India

Douglas J. Gardner, MD, Toronto, Ontario, Canada

Bradley S. Gluck, MD, Southampton, NY

Mark G. Goldshein, MD, Andover, MA

Juan Jose Gomez Muga, MD, Vitoria, Spain

Alvaro Gomez Naar, MD, Salta Capital, Argentina

Taku Gomi, Tokyo, Japan

Preetam Gongidi, DO, Philadelphia, PA

Wataru Gonoi, MD, PhD, Bunkyo-ku, Japan

Pramod K. Gupta, MD, Plano, TX

Akifumi Hagiwara, MD, Tokyo, Japan

D. C. Heasley, Jr, MD, Dallas, TX

Christoph Hefel, Feldkirch, Austria

Yuusuke Hirokawa, MD, Kyoto, Japan

Shintaro Ichikawa, MD, Chuo-City, Japan

Mitsuru Ikeda, MD, Nagoya, Japan

Richard N. Irion, MD, South Jordan, UT

Stephen F. Janas, MD, De Pere, WI

Kiriakos Kalampoukas, MD, Halandri, Greece

Koki Kato, MD, Utsunomiya, Japan

Dennis Kies, MD, Valkenburg, the Netherlands

Takao Kiguchi, MD, Ichinomiya, Japan

Osamu Kizu, MD, Ohtsu, Japan

Mitchell A. Klein, MD, Mequon, WI

Masamichi Koyama, MD, PhD, Tokyo, Japan

Glenn A. Krinsky, MD, Upper Saddle River, NJ

Mario A. Laguna, MD, Franklin, WI

Acrane Y. Li, MBChB, Auckland, New Zealand

David A. Lisle, MBBS, Brisbane, Australia

Rafael Maffei Loureiro, MD, Sao Paulo, Brazil

Stephen V. Manghisi, MD, Closter, NJ

Satoshi Matsushima, MD, Tokyo, Japan

Manabu Minami, MD, PhD, Yokohama, Japan

Clara Morandeira, MD, Bilbao, Spain

Adriana C. Moreira, MD, Porto, Portugal

Kyoko Nagai, MD, Yokohama, Japan

Ryusuke Nakamoto, MD, Kyoto, Japan

Armin Neff, MD, Speicher, Switzerland

Tammam N. Nehme, MD, Mattawan, MI

Nariman Nezami, MD, New Haven, CT

Soheil Niku, MD, Carlsbad, CA

Tomokazu Nishiguchi, MD, PhD, Cairns, Australia

Roque Oca, MD, Bilbao, Spain

Ryusuke Ookura, MD, Kobe, Japan

Michael D. Orsi, MD, San Antonio, TX

Vishal Panchal, MD, San Francisco, CA

David M. Panicek, MD, New York, NY

Ioannis E. Papachristos, MD, Agrinio, Greece

Suresh K. Patel, MD, Chicago, IL

Narendrakumar P. Patel, MD, Newburgh, NY

Sudhakar N. Pipavath, MD, Seattle, WA

Adilson Prando, MD, Campinas, Brazil

Shawn P. Quillin, MD, Charlotte, NC

Daniel C. Rappaport, MD, Toronto, Ontario, Canada

Mantosh S. Rattan, MD, Cincinnati, OH

Rahul D. Renapurkar, MD, Cleveland, OH

Daniel Romeu Vilar, MD, Bertamirans, Spain

Kunihiro Saeki, Sao Paulo, Brazil

Akihiko Sakata, MD, Kyoto, Japan

Yusuke Sakurai, Nagoya, Japan

Abdullah Sariyildirim, II, MD, Osmaniye, Turkey

Shakil Sarwar, MBBS, Gujranwala, Pakistan

Kohei Sasaguri, MD, Saga, Japan

Shuichi Satoh, MD, Oota-ku, Japan

Andrew Schapiro, MD, Cincinnati, OH

Meir H. Scheinfeld, MD, PhD, Suffern, NY

Steven M. Schultz, MD, Fort Worth, TX

Anthony J. Scuderi, MD, Johnstown, PA

Matthew P. Shapiro, MD, Charlottesvle, VA

Taro Shimono, MD, Osaka, Japan

Paul J. Shogan, MD, Burlington, IA

Grady V. Shue, Jr, MD, Hickory, NC

Michael S. Siegfried, MD, Glencoe, IL

David F. Sobel, MD, La Jolla, CA

Luis A. Sosa, MD, Mexico City, Mexico

James D. Sprinkle, Jr, MD, Spotsylvania, VA

Paul Stark, MD, La Jolla, CA

Hongliang Sun, MD, Beijing, China

David M. Tabriz, MD, Gainesville, FL

Taku Tajima, MD, Bunkyo-ku, Japan

Hiroaki Takahashi, MD, Tokyo, Japan

Gregory P. Tarr, MBChB, PhD, Auckland, New Zealand

Shanigarn Thiravit, MD, Muang Nonthaburi, Thailand

Eugene Tong, MD, Austin, TX

Stamos J. Trakadas, MD, Athens, Greece

Scott S. Tsai, MD, Oakville, Ontario, Canada

Jeffrey Tseng, MD, Menlo Park, CA

Meric Tuzun, MD, Ankara, Turkey

Edith V. Vassallo, MD, Marsaskala, Malta

Ainhoa Viteri, MD, Brooklyn, NY

Christopher P. Vittore, MD, Belvidere, IL

Haruo Watanabe, MD, Gifu, Japan

Jeffrey H. West, MD, Jacksonville, FL

Joseph L. Whetstone, MD, Hood River, OR

Yi-Wei Wu, MD, Singapore

George S. Wu, MD, Danville, PA

Takayuki Yamamoto, MD, Kyoto, Japan

Mihoko Yamazaki, MD, Higashimatsuyama, Japan

Satoru Yoshida, MD, PhD, Muroran, Japan

Kaneko You, Gifu, Japan

Dahua Zhou, MD, Old Westbury, NY

Ahmed Zidan, MD, Barcelona, Spain

Resident group responses

Brigham and Women’s Hospital Radiology Residents, Boston, MA

Hospital de Santa Maria Radiology Residents, Lisbon, Portugal

Mater Dei Hospital Radiology Residents, Msida, Malta

Mie University Hospital Radiology Residents, Tsu, Japan

Montefiore Medical Center Radiology Residents, Bronx, NY

Prince of Songkla University Radiology Residents, Songkhla, Thailand

Tsukuba University Hospital Radiology Residents, Tsukuba, Ibaraki, Japan

University of Pennsylvania Radiology Residents, Philadelphia, PA